Porphyromonas gingivalis has been shown to employ varied virulence strategies in its contribution to periodontal and systemic diseases. Some of the key virulence mechanisms include host cell invasion, modulation of inflammatory mediators, complex biofilm formation, resistance to host killing mechanisms, production of damaging proteases and inducing shifts in the commensual microbial community toward a pathogenic one. Surface polysaccharides are known to play critical roles in such mechanisms in many bacterially associated diseases. The polysaccharide portion of P. gingivalis lipopolysaccharide (LPS-PS) forms a large highly complex array of structures on the bacterial cell surface. Its complexity and exposure on the bacterial surface suggest an important role (or roles) in pathogen-host interactions. In spite of this, only the lipid moiety that anchors the polysaccharide into the cell membrane (lipid A) has been extensively examined for a role in pathogenesis. This application seeks to examine two previously undiscovered roles for this class of surface glycan in P. gingivalis pathogenesis. Aim 1 will examine the role of LPS-PS in host cell invasion, a role which has been shown to be important for invasion in numerous bacteria, but no oral species have been examined. Aim 2 will explore how LPS-PS affects host cell inflammatory response, a role that has not been clearly demonstrated in any bacterium.